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SRK2E/OST1/SnRK2.6的调控结构域与ABI1相互作用,并整合脱落酸(ABA)和渗透胁迫信号,从而控制拟南芥气孔关闭。

The regulatory domain of SRK2E/OST1/SnRK2.6 interacts with ABI1 and integrates abscisic acid (ABA) and osmotic stress signals controlling stomatal closure in Arabidopsis.

作者信息

Yoshida Riichiro, Umezawa Taishi, Mizoguchi Tsuyoshi, Takahashi Seiji, Takahashi Fuminori, Shinozaki Kazuo

机构信息

Laboratory of Plant Molecular Biology, RIKEN Tsukuba Institute, 3-1-1, Koyadai, Tsukuba, Ibaraki 305-0074, Japan.

出版信息

J Biol Chem. 2006 Feb 24;281(8):5310-8. doi: 10.1074/jbc.M509820200. Epub 2005 Dec 19.

Abstract

ABI1 and ABI2 encode PP2C-type protein phosphatases and are thought to negatively regulate many aspects of abscisic acid (ABA) signaling, including stomatal closure in Arabidopsis. In contrast, SRK2E/OST1/SnRK2.6 encodes an Arabidopsis SnRK2 protein kinase and acts as a positive regulator in the ABA-induced stomatal closure. SRK2E/OST1 is activated by osmotic stress as well as by ABA, but the independence of the two activation processes has not yet been determined. Additionally, interaction between SRK2E/OST1 and PP2C-type phosphatases (ABI1 and ABI2) is not understood. In the present study, we demonstrated that the abi1-1 mutation, but not the abi2-1 mutation, strongly inhibited ABA-dependent SRK2E/OST1 activation. In contrast, osmotic stress activated SRK2E/OST1 even in abi1-1 and aba2-1 plants. The C-terminal regulatory domain of SRK2E/OST1 was required for its activation by both ABA and osmotic stress in Arabidopsis. The C-terminal domain was functionally divided into Domains I and II. Domain II was required only for the ABA-dependent activation of SRK2E/OST1, whereas Domain I was responsible for the ABA-independent activation. Full-length SRK2E/OST1 completely complemented the wilty phenotype of the srk2e mutant, but SRK2E/OST1 lacking Domain II did not. Domain II interacted with the ABI1 protein in a yeast two-hybrid assay. Our results suggested that the direct interaction between SRK2E/OST1 and ABI1 through Domain II plays a critical role in the control of stomatal closure.

摘要

ABI1和ABI2编码PP2C型蛋白磷酸酶,被认为对脱落酸(ABA)信号传导的多个方面起负调控作用,包括拟南芥中的气孔关闭。相反,SRK2E/OST1/SnRK2.6编码一种拟南芥SnRK2蛋白激酶,在ABA诱导的气孔关闭中起正调控作用。SRK2E/OST1可被渗透胁迫以及ABA激活,但这两个激活过程的独立性尚未确定。此外,SRK2E/OST1与PP2C型磷酸酶(ABI1和ABI2)之间的相互作用也不清楚。在本研究中,我们证明abi1 - 1突变而非abi2 - 1突变强烈抑制ABA依赖的SRK2E/OST1激活。相反,即使在abi1 - 1和aba2 - 1植物中,渗透胁迫也能激活SRK2E/OST1。在拟南芥中,SRK2E/OST1的C末端调节结构域是其被ABA和渗透胁迫激活所必需的。C末端结构域在功能上分为结构域I和结构域II。结构域II仅对SRK2E/OST1的ABA依赖激活是必需的,而结构域I负责ABA非依赖激活。全长SRK2E/OST1完全互补了srk2e突变体的萎蔫表型,但缺少结构域II的SRK2E/OST1则不能。在酵母双杂交试验中,结构域II与ABI1蛋白相互作用。我们的结果表明,SRK2E/OST1与ABI1通过结构域II的直接相互作用在气孔关闭的控制中起关键作用。

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